RESUMO
The mechanisms that control TNF-á production by macrophages during Trypanosoma cruzi infection are still unknown. Destruction of intracellular forms by cytokine activated macrophages is considered to be a major mechanism of parasite elimination. Although in vitro TNF-á contributes to enhanced parasite destruction by macrophages, previous work in vivo has shown that as the parasite burden increases, serum TNF-á levels decline. In this report we show that TNF-á production by peritoneal adherent cells is elevated at the initial phase of T. cruzi infection. As infection progresses TNF-á production decreases. The observed reduction is partly due to inhibition, largely exerted by endogenous PG and secondarily by NO. Inhibition of their synthesis partially restored the ability to produce high levels of TNF-á to macrophages upon stimulation by LPS. Neither endogenous IL-10 nor TGF-â seem to be involved in the negative regulation of TNF-á production.